Zoe Feigen (final year student, University of Sydney) and Diane Ryan (Elizabeth MacArthur Agricultural Institute, Menangle) and Bruce Watt (Central Tablelands Local Lands Services, Bathurst)

Posted Flock & Herd January 2014


Epizootic Haemorrhagic Disease (EHD) is viral disease, primarily of ruminants. Overseas, it causes severe disease in cervids and is associated with mild disease in cattle and bighorn sheep and carrier states in domestic sheep, goats and other wild ungulates (EFSA 2009). EHD virus is closely related to bluetongue virus (EFSA 2009).

Some importing countries request certification for the EHD status of Australian alpacas. While alpacas may contract bluetongue there is no evidence to suggest that they are susceptible to EHD.


EHD is caused by an Orbivirus of the family Reoviridae. The diseases caused by both EHD and bluetongue present with similar clinical signs and are together classed as haemorrhagic diseases. EHDV is usually spread by Culicoides midges (EFSA 2009). It is therefore mostly a disease of late summer and early autumn, coinciding with warm, moist conditions. Six of the ten serotypes of EHD have been reported in Australia, including EHDV-1, the serotype associated with significant disease overseas (Weir et al. 1997). White-tailed deer (Odocoileus virginianus) and other wild deer are most commonly affected by EHDV-1 with high mortalities occurring in the USA where these species are common (EFSA 2009; Iowa State University 2012). The Australian strain of EHDV-1 has been found to be 20% different on a nucleotide basis to the North American version and has not been associated with significant animal mortalities (Weir et al. 1997). Other serotypes reported in Australia are 2, 5, 6, 7 and 8, with 2 and 5 being the most commonly detected (Weir et al. 1997). Serotype 7 has been associated with disease in cattle overseas but is considered non pathogenic in Australia (EFSA 2009; Weir et al. 1997). Serotypes 2, 5, 6 and 8 are associated with mild disease.


Deer may show one of three syndromes associated with EHD infection (EFSA 2009; Iowa State University 2012). Deer experiencing peracute disease often die prior to the development of significant clinical signs. Death is usually within 8-36 hours of contracting the virus. If clinical signs are observed they can include pyrexia, anorexia, weakness, respiratory distress, swelling of the tongue and conjunctiva and oedema of the head and neck. These clinical signs are also seen in the acute form of the disease and may be accompanied by extensive haemorrhage of the skin, heart and gastrointestinal tract. Haemorrhage of the pulmonary vessels is considered pathognomonic for EHD and bluetongue with the virus binding to receptors in this region, resulting in bleeding into the endothelium. Acutely affected animals may show signs of excessive and often haemorrhagic salivation and nasal discharge. Ulcers and erosions of the tongue, dental pad, palate, rumen and omasum are also common. The peracute and acute forms of EHD often result in high mortality rates, with die-offs of up to 90% of deer populations recorded in the United States. Chronically affected deer will develop ulcerations and erosions of the lining of the rumen. Scarring of the rumen will prevent proper digestion and lead to emaciation over a period of many weeks. Additionally, severely affected animals may develop laminitis with sloughing of the hoof walls. Chronic infections may present similar to severely laminitic animals with bluetongue. Deer may crawl on their chest to avoid standing on painful feet (Iowa State University 2012).


Overseas, cattle are less severely affected than deer and outbreaks are usually associated with low mortalities and morbidities of 1-18% (EFSA 2009). More severely affected animals can be ill thrifty for a prolonged period. Clinical disease in cattle is characterised by pyrexia, anorexia, dehydration and dysphagia resulting from damage to the striated muscles of the tongue, pharynx, larynx and oesophagus. Animals may develop aspiration pneumonia and become emaciated. Ulceration of the oral cavity is common in addition to oedema, haemorrhage and erosive lesions of the lips and coronary band of the hooves. Similar to chronic EHD in deer, cattle may develop lameness. Pregnant cows infected between 70 and 120 days of gestation may resorb the foetus, or the fetus may develop hydranencephaly (EFSA 2009; Iowa State University 2012).

EHD infection and viraemia has been recorded in sheep; however clinical disease has not been reported (EFSA 2009; Iowa State University 2012). Experimental infection of domestic goats has not resulted in a viraemia (Iowa State University 2012).


Until recently, it was believed that haemorrhagic disease viruses did not cause clinical disease in South American camelids. In 2000, an import risk analysis by the Department of Agriculture, Forestry and Fisheries (Australian Quarantine Inspection Service 2000) stated that while antibodies to bluetongue virus have been found in alpacas, there had been no cases of clinical disease of bluetongue or reports to suggest that alpacas could be infected with EHD virus. This assessment changed following the northern European bluetongue pandemic of 2006-2008, where a fatal case of bluetongue was recorded in an alpaca (Henrich, Reinacher & Hamann 2007). A subsequent case has been recorded in California, also associated with a severe outbreak of bluetongue in sheep (Ortega et al. 2010). Clinically, bluetongue in alpacas presented similarly to deer with the peracute form of EHD, with inappetence, weakness and respiratory distress (Henrich, Reinacher & Hamann 2007; Ortega et al. 2010). Death occurred within 24 hours of clinical signs developing. Post-mortem findings in these cases showed diffuse pulmonary oedema but, with erosive oral lesions in the European case (Henrich, Reinacher & Hamann 2007) and focal haemorrhages of the myocardium occurring in the Californian case (Ortega et al. 2010). The pathognomonic haemorrhage of the pulmonary vessels in other species was not observed. Bluetongue infection was diagnosed by PCR (Henrich, Reinacher & Hamann 2007; Ortega et al. 2010).

While these cases show that it is possible for alpacas to be infected by bluetongue virus and develop clinical signs there is still no evidence to suggest that they are susceptible to EHD. There have been suggestions that the bluetongue virus and the EHD virus may be capable of recombination due to the genetic similarity of the two viruses. However, this recombination has only been demonstrated in the laboratory (Blois et al. 1991). Therefore, the risk of alpacas becoming susceptible to EHD through mutation of the EHD virus is low. In addition, it is likely that alpacas are only susceptible to bluetongue during outbreaks of highly pathogenic strains of the virus in other species.


  1. Australian Quarantine and Inspection Service 2000, 'Import risk analysis for the importation of camelids from Chile and Peru', AQIS Canberra
  2. Blois, HL, Fayard, B, Urakawa, T, Roy, P 1991, 'Synthesis and Characterization of Chimeric Particles between Epizootic Hemorrhagic Disease Virus and Bluetongue Virus: Functional Domains Are Conserved on the VP3 Protein', Journal of Virology, vol 65, no 9, pp 4821-4831
  3. EFSA Panel on Animal Health and Welfare (AHAW) 2009, 'Scientific Opinion on Epizootic Hemorrhagic Disease', EFSA Journal, vol 7, no 12, 67 pp
  4. Henrich, M, Reinacher, M, Hamann, HP 2007, 'Lethal bluetongue virus infection in an alpaca', Veterinary Record, vol 161, p 764
  5. Iowa State University College of Veterinary Medicine 2012, 'Epizootic hemorrhagic disease (EHD) in deer and cattle', viewed 10.5.13 See
  6. Ortega, J, Crossley, B, Dechant, JE, Drew, CP, MacLachlan, NJ 2010, 'Fatal Bluetongue Virus Infection in an Alpaca (Vicugna Pacos) in California', Journal of Veterinary Diagnostic Investigation, vol 22, pp 134-136
  7. Weir, RP, Harmsen, MB, Hunt, NT, Blacksell, SD, Lunt, RA, Pritchard, LI, Newberry, KM, Hyatt, AD, Gould, AR, Melville, LF 1997, 'EHDV-l, a new Australian serotype of epizootic haemorrhagic disease virus isolated from sentinel cattle in the Northern Territory', Veterinary Microbiology, vol 58, pp 135-143


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